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Heart failure is a clinical complex syndrome of symptoms and signs resulting from any structural or functional cardiac disorder. Untreated it has a poor prognosis, but this can be improved considerably with early and optimal treatment. The most common causes of heart failure in our country is coronary artery disease (CAD) and non-ischemic causes of systolic dysfunction and may have an identifiable cause (e.g., hypertension (HT), valvular disease, myocardial toxins, or myocarditis) or may have no prominent cause (e.g., idiopathic dilated cardiomyopathy).Patients with HF are almost equally divided into those with impairment of left ventricular blood ejection (systolic dysfunction) those with preserved ejection fraction(EF) and impairment of the tendency of the ventricle to fill with (diastolic dysfunction). The result of either type of HF is decreased cardiac output (CO). Less blood is pumped from the heart to the body. Decreased CO also can lead to decreased blood pressure (BP). Although the systolic function is reduced or not, most of the current evidence on drug treatment is for HF due to left ventricular systolic dysfunction. The cardiac manifestations of HF are dyspnea and fatigue, which may reduce exercise ability, and fluid accumulation, which may cause to pulmonary (fluid backing up in the lungs) and peripheral edema.
The classification system that is most commonly used to quantify the amount of functional limitation assumed by HF is presented. This system divide patients to 1 of 4 functional classes depending on the degree of effort needed to elicit symptoms, only at levels that would limit normal individuals (class I), on ordinary exertion (class II), on less-than-ordinary exertion (class III), patients might have features of HF at rest (class IV). But functional classification reflects the subjective assessment of physician and patient. The principal manifestation of the HF such progression is a process known as remodeling which occurs as a homeostatic attempt to decrease wall stress, through increases in wall thickness. This ultimately results in a change in the geometry of the left ventricle (LV) such that the chamber dilates, hypertrophies, and becomes more spherical. The process of cardiac remodeling generally precedes the development of symptoms. The process of remodeling continues after the appearance of symptoms and may contribute importantly to worsening of symptoms despite treatment. Heart failure is a very common disease that can have a high death rate. Despite advancements in treatment, the death rate has been increasing. Therefore, understanding the disease mechanism and its progression, common causes, risk factors, signs and symptoms, and treatments are very important.
A state in which heart fails to maintain an adequate circulation (CO) for the needs of body, despite a satisfactory venous filling (VF) pressure.( by definition excludes those condition in which the CO is low due to decreased venous filling pressure like in hypo volaemic shock condition)
Acute and chronic HF
Left ventricular, right ventricular & biventricular(congestive) HF
HF due to Systolic dysfunction & Diastolic dysfunction
Forward failure & Back ward failure
High output failure & Low output failure
The New York Heart Association (NYHA) classification is the most widely used
Stratification tool for assigning patients with CHF to functional classes
Class I No limitation of activities
Class II Slight, mild limitation of activity
Class III Marked limitation of activity
Class IV Activity severely limited
This stage identifies patient who has high adventure for developing HF, since they have one or more risk factors, but they do not have structural disorders of the heart.
This stage refers to patients who, despite a structural disorder of the heart, have never developed symptoms of HF.
This stage shows patients with past or current features of HF
This stage shows patients with late-stage disease who need special treatment strategies like mechanical circulatory help, continuous inotropic infusions, cardiac tra
When the HF, considerable changes occur to the heart and peripheral vascular system in response to the haemodynamic changes associated with HF .These physiological changes are compensatory and maintain CO and peripheral perfusion. However, as HF progresses, these mechanisms are overwhelmed and become pathophysiological. The development of pathological peripheral vasoconstriction and sodium retention in heart failure by activation of the renin-angiotensin-aldosterone system are a loss of beneficial compensatory mechanisms and represent cardiac decompensation. Factors involved are venous return, outflow resistance, contractility of the myocardium, and salt and water retention.
Causes of heart failure
Ischaemic heart disease (35-40%)
Cardiomyopathy (dilated) (30-34%)
Hypertrophic or obstructive
Restrictive (amyloidosis, sarcoidosis)
Valvular heart disease
Mitral stenosis & regurgitation
Aortic stenosis & regurgitation
Tricuspid stenosis & regurgitation
Congenital heart disease
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Alcohol and drugs
Right heart failure
cor pulmonale (COPD)
(HF can involve primarily the right ventricle)
Ventricular fibrillation & flutter
complete heart block
the sick sinus syndrome
Pathophysiological changes in HF are seen,
Altered myosin gene expression
Decreased myosin ATP activity
Changes in isoforms of myosin
Abnormal actin & tropomyosin synthesis
Decreased beta adrenergic receptors on myocardium
Altered sarcoplasmic Ca2+ -ATPase density
Slow relaxation of myocardium & it contri bute to diastolic dysfunction
Increased atrial natriuretic peptide (ANP) secretion
Increased collagen synthesis
This is due to high work load
This is adaptive mechanism.
This is due to sympathetic activity.
Salt and water retention
This is due to reduced renal perfusion
Physiological factors affecting CO are very important in HF,
Heart rate(HR) :
autonomic nervous system
Preload (Venous return)(VR)
Stretching the myocardial fibers during diastole is the preload (end diastolic stretching).End diastolic volume(EDV) or end diastolic venous filling pressure affect on preload. Failure of myocardium leads to a reduction of the volume of blood ejected with each heartbeat and an increase in the volume of blood remaining after systole. This increased EDV stretches the myocardial fibres.
Afterload (Outflow resistance)
It can be expressed as tension which is developed in the wall of ventricles during systole to open the semilunar valves and ejection of blood to aorta & pulmonary arteries in both sides of heart. According to Laplace law,
Intraventricular pressure x radius of ventricle
Wall tension = --------------------------------------------------------
2 x ventricular wall thickness
Increased afterload is due to
elevation of arterial resistance
increased ventricular size
Decreased afterload is due
decreased arterial resistance
decreased ventricular size
An increase in afterload decreases the cardiac output. This results in a further increase of EDV and dilatation of the ventricle itself, which further arouse the problem of afterload. This is expressed by,
Laplace's law: the tension of the myocardium (T) is proportional to the intraventricular pressure (P) multiplied by the radius of the ventricular chamber.
Changes in ability of myocardium to develop the force of contraction that occur independently on the changes in myocardial fibre length. The sympathetic nervous system is activated in heart failure via baroreceptors as an early compensatory mechanism, which provides inotropic support and maintains cardiac output. Chronic sympathetic activation, however, has harmful effects by further increasing neurohormonal activation and myocyte apoptosis. This is compensated by a down regulation of Î²-receptors.
Factors involved in contractile state of myocardium,
Digitalis & other inotropic effects
Loss of myocardium
Sympathetic & parasympathetic nerve impulses
Hypoxia, Hypercapnea, Acidosis
Myocardial remodeling in heart failure
LV remodelling is a process of progressive alteration of ventricular shape, size and function owing to the impact of neurohormonal, mechanical and possibly genetic factors in several clinical conditions, including myocardial infarction(MI), cardiomyopathy, HT, and valvular heart disease. Its include hypertrophy, loss of myocytes, and increased interstitial fibrosis. Remodelling continues for months after the initial insult, and the ultimate change in the shape of the ventricle becomes responsible for significant impairment of overall function of the heart as a pump. In cardiomyopathy, the process of progressive ventricular dilatation or hypertrophy occurs without ischemic myocardial injury or infarction.
CLINICAL SYNDROMES OF HEART FAILURE
There are many clinical syndromes are go with HF,
Forward failure theory
Back ward failure theory
Left heart failure
Ischaemic heart disease(IHD) (the most common reason)
Systemic hypertension (chronic)
Mitral and Aortic valve disease-
( Mitral stenosis causes left atrial hypertension)
paroxysmal nocturnal dyspnoea
Auscultation detects a left ventricular third or fourth heart sound
Tachycardia (gallop rhythm)
Crackles are heard at the lung bases
Right heart failure
Chronic lung disease (cor pulmonale)
Isolated right ventricular cardiomyopathy
Left-to-right shunts (ASD,VSD)
Mitral valve disease with pulmonary hypertension
Pulmonary embolism or pulmonary hypertension
Pulmonary valve disease
Tricuspid valve disease
Dependent pitting oedema
free abdominal fluids are produced (ascites)
Jugular venous distension (plus or minus v waves of tricuspid regurgitation)
Pleural transudates (right plura)
All most all HF are congestive heart failure. This is due to diseases affecting both ventricles. Long lasting left ventricular failure causes to right ventricular failure resulting congestive HF. Congestive heart failure is a syndrome that can be caused by multiple underlying diseases
Congenital heart disease
Chronic rapid heart beat
Left or right-sided failure
1.Involve in gravity:
Orthopnea (shortness of breath when lying down position)
Shortness of breath during exertion
2. Involving circulation
Fatigue or weakness
Rapid or irregular heart beat
Changes of behavior (restlessness, confusion, and decreased attention span)
Systolic ventricular failure is most commonly due to,
The left ventricle is normally dilated and fails to contract normally.
Forward failure theory, this due to inadequate CO at rest or with exercise stress results in decreased perfusion to vital organs.
Back ward failure theory, This due to decreased contractility results in increased LV diastolic pressure causing fluid buildup in the pulmonary vasculature.
Gallops (third heart sound)
Increased Jugular venous pressure
Diastolic heart failure
Diastolic HF results from impaired relaxation of myocardium. Ventricular wall stiffness is increased and left ventricular compliance is decreased. This leads to impairment of diastolic ventricular filling and then CO is decreased. CAD, HT and hypertrophic cardiomyopathy are common causes. Amyloid may lead to diastolic dysfunction.
High-output heart failure
The heart is unable to supply the conditions like anemia, beriberi, and thyrotoxicosis. This HF is like low-output condition but is associated with tachycardia and a gallop rhythm. Patients are often warm with distended superficial veins. Unlike low-output failure, the oxygen content of systemic venous blood is high owing to the delivery of large amounts of arterial blood to non-metabolizing tissues.
Chronic heart failure
Making an accurate diagnosis of HF and determining its cause can be difficult. Clinical diagnosis is confirmed to be accurate in approximately half of cases when investigated by echocardiography. The probability of HF in the presence of suggestive symptoms and signs is increased if there is a history of MI or angina, an abnormal ECG, or a chest X-ray showing pulmonary congestion or cardiomegaly.
Decreased exercise tolerance
Orthopnoea ankle swelling
Paroxysmal nocturnal dyspnea
Shortness of breath on exertion
Acute Heart Failure
Acute HF is characteristic with acute (cardiogenic) dyspnoea characterized by signs which cause to pulmonary congestion. It is suitable to name as acute pulmonary oedema or cardiogenic shock.
Acute HFof the heart most commonly occurs in the setting of acute myocardial infarction when there is extensive loss of ventricular muscle. The condition may also occur with rupture of the interventricular septum producing a ventricular septal defect, or be due to acute valvular regurgitation. Common examples of valvular regurgitation are papillary or chordal rupture producing mitral regurgitation, or sudden aortic valve regurgitation in infective endocarditis. Other causes of acute heart failure include obstruction of the circulation by acute pulmonary embolus and cardiac tamponade. In each case severe cardiac failure can occur with a relatively normal heart size.
DIAGNOSIS OF HEART FAILURE
The diagnosis of HF depends on history and clinical information. It is wanted evidence of cardiac dysfunction with relevant investigation with the help of echocardiography.
Investigations are wanted to diagnose it, they are two types,
Full blood count(FBC)
Urea and electrolytes imbalance
Pulmonary congestion checking
Intra cardiac thrombus.
Radionuclide angiography (RNA)
Single photon emission computed tomography (SPECT)
Positron emission tomography (PET).
Ambulatory (24-48 hours) ECG.
Cardiopulmonary exercise testing.
Resting and stress radionuclide angiography
TREATMENT OF HF AND THEIR PHYSIOLOGIC BASIS
Treatment is 2 divisions,
Normal life behavior advice
Angiotensin receptor antagonists
Angiotensin-converting enzyme inhibitors (ACEI)
vasodilators of arterioles
Î’-Adrenoceptor blocking agents
Non-pharmacological treatment of HF
Normal life behavior advice
Large meals are not suitable.
Weight reduction is wanted
Salt limitation is needed.
Alcohol is dangerous(because it has negative inotropic effect)
Counseling programs are important. Patient should be having knowledge about diet, drugs, and exercises.
Body mass index should be kept on normal level.
Physical activities & exercises
Not suitable sildenafil like drugs which are include nitrates.
Smoking should be stopped
Arrhythmias are frequent in HF and are implicated in sudden death. Although treatment of complex ventricular arrhythmias might be expected to
Improve survival, there is no evidence to support this and I may increase mortality.
Patients require prophylactic anticoagulation. HF is associated with a four-fold increase in the risk of a stroke. Oral anticoagulants are recommended in patients with atrial fibrillation (AF) and in patients with sinus rhythm with a history of thromboembolism, left ventricular thrombus or aneurysm. In patients with known IHD,
antiplatelet therapy- (aspirin, clopidogrel)
Diuretics develop the renal excretion of salt and H2O by blocking tubular reabsorption of Na+ and Cl-. Fluid loss reduces ventricular filling pressures (preload) and produces certain haemodynamic and symptoms in patients with HF and also quickly develops dyspnoea and peripheral oedema. The intravenous administration of loop diuretics (furosemide) relieves pulmonary oedema quikly with the help of arteriolar vasodilatation reducing afterload.
Diuretics are many types,
Loop diuretics like bumetanide and furosemide have a quick onset of action. Concentrating power of the kidney is decreased. Loop diuresis also produces marked K+ loss and develops hyperuricaemia.
Potassium excretion is put on. Thiazides are less effective in patients with reduced glomerular filtration rate (GFR). Thiazide diuretics together with loop diuretics have a higher diuretic effect. But their use may be complicated by over diuresis and electrolyte depletion. Consequence of complication,
Intravenous inotropes are always used to treat myocardial function in patients with acute left ventricular failure. Dobutamine, Dopexamine and Dopamine are intravenous adrenergic agonists.
Digitalis glycosides have been used for many years in patients with HF and atrial fibrillation. A little increase in deaths inferred to be secondary to MI. So patients who are presented with severe HF despite therapy with vasodilators, diuretics should have digoxin .It is partly protein-bound. Most of our excreted with urine. Its accumulation can occur in renal failure. It has positive inotrope effect Digoxin also improves baroreceptor responsiveness, and reduces sympathetic activity and circulating renin. Anorexia, nausea, altered vision are present in digoxine toxicity. Digoxin toxicity is treated by stopping the drug, restoration of serum potassium and management of arrhythmias.
It depends on the representation that the inotropic state of the failing myocardium is impaired and that the myocardial response to adrenergic stimulation is reduced. Several adrenergic agonists have been examined in HF. These agents surely increase mortality.
Diuretics and sodium restriction carry out to activate the renin-angiotensin system, stimulate formation of angiotensin. A difference of other neural and hormonal reactions serves to increase preload and afterload. These compensatory mechanisms are fruitful in supporting BP ,BF. Also HF reduces CO. The high venous pressures found in HF are also related to the activation of the sympathetic nervous system, arrival of circulating vasoconstrictors, shifting the Frank Starling curve to the right.
Angiotensin receptor antagonists
Angiotensin II receptor antagonists have equal hemodynamic effects to ACEI, where as they do not affect bradykinin metabolism.
Dilators of arterioles
Drugs like Î±-adrenergic blockers (prazosin) and direct smooth-muscle relaxants (e.g. hydralazine) are potent arteriolar vasodilators, where as they are not very effective in HF. Afterload is reduced by Calcium-channel blockers, but first-generation calcium antagonists (diltiazem, nifedipine) may have a baneful action on left ventricular function in HF.
Angiotensin converting enzyme inhibitors
ACEI has lower systemic vascular resistance and venous pressure. It reduces levels of circulating catecholamines. The useful hemodynamic effect of these drugs represents to be independent of their inhibition of ACE. Some of these agents are pro-drugs (e.g. enalapril).These drugs have a delayed of action and first-dose hypotension may not occur.Pre drugs are better avoided if HF results in altered hepatic function. Engaged potassium-sparing diuretics should be discontinued .ACEI tend to raise potassium retention. A forthcoming examination looking at dose and entity.
glycerol trinitrate and isosorbide mononitrate act by decreasing preload and lowering venous pressure, with resulting reduction in pulmonary and dependent oedema. Reduction of filling pressure doesn't augment CO. combination therapy of nitrate with hydralazine has been shown to develop mortality and exercise accomplishment, and may be salutary when ACEI are contra indicated. The advantage of vasodilators is not as great as with ACEI.
Î²-Adrenoceptor blocking agents
There is sufficient testimony to support the use of beta-blockers in patients with chronic HF. The non-selective vasodilator beta-blocker with additional vasodilator and antioxidant has demonstrated a significant progress in mortality. Following the administration of beta-blockers, the EF decline, whereas normally returns to base line. Patients who are in HF and already on treatment with a beta-blocker for a coexisting situation like CAD or HT.
Non-pharmacological treatment of heart failure
patients with sinoatrial disease and atrioventricular conduction block are needed this. Pacemakers are alsoimportant in patients without AV block whereas with prolonged PR intervals.Biventricular pacing should also be considered in patients not responding to therapy in situations like systolic heart failure,optimal medical therapy ,sinus rhythm, atrial fibrillation, mitral regurgitation.
Cardiac transplantation has been the treatment for patients with severe intractable HF.The availability of heart transplantation is limited.Heart do not function usually. Cardiac denervation results in a high resting HR, loss of daily blood pressure variation and impaired renin-angiotensin-aldosterone system. The complications of heart transplantation are,
Allograft vascular diseases
There are specific contraindications to cardiac transplantation,
Alcohol or drug abuse
High pulmonary vasculature resistance
Severe renal or liver failure
Uncontrolled psychiatric illness
Left ventricular assist device and artificial heart
Left ventricular assist devices and Artificial hearts are used to transplantation surgery. Mechanical devices are also mentioned if there is a ability of auto recovery.